Ascunce Karina, Dhodapkar Rahul M, Huang Deven, Hafler Brian P
Interdepartmental Neuroscience Program, Yale University, New Haven, CT, United States.
Department of Ophthalmology, Roski Eye Institute, University of Southern California, Los Angeles, California.
Front Cell Dev Biol. 2023 Feb 28;11:1118524. doi: 10.3389/fcell.2023.1118524. eCollection 2023.
Age-related macular degeneration (AMD) is a neurodegenerative disease and a leading cause of irreversible vision loss in the developed world. While not classically described as an inflammatory disease, a growing body of evidence has implicated several components of the innate immune system in the pathophysiology of age-related macular degeneration. In particular, complement activation, microglial involvement, and blood-retinal-barrier disruption have been shown to play key roles in disease progression, and subsequent vision loss. This review discusses the role of the innate immune system in age-related macular degeneration as well as recent developments in single-cell transcriptomics that help advance the understanding and treatment of age-related macular degeneration. We also explore the several potential therapeutic targets for age-related macular degeneration in the context of innate immune activation.
年龄相关性黄斑变性(AMD)是一种神经退行性疾病,也是发达国家不可逆视力丧失的主要原因。虽然传统上不被描述为炎症性疾病,但越来越多的证据表明,先天性免疫系统的几个组成部分与年龄相关性黄斑变性的病理生理学有关。特别是,补体激活、小胶质细胞参与和血视网膜屏障破坏已被证明在疾病进展及随后的视力丧失中起关键作用。本综述讨论了先天性免疫系统在年龄相关性黄斑变性中的作用,以及单细胞转录组学的最新进展,这些进展有助于推动对年龄相关性黄斑变性的理解和治疗。我们还在先天性免疫激活的背景下探讨了年龄相关性黄斑变性的几个潜在治疗靶点。